Osteoarthritis (OA) is the most common form of joint disease. 

Although OA was previously thought to be a progressive, degenerative disorder, it is now known that spontaneous arrest or reversal of the disease can occur. 

Conventional medications are often effective for symptom relief, but they can also cause significant side effects and do not slow the progression of the disease. 

Several natural substances have been shown to be at least as effective as nonsteroidal anti-inflammatory drugs at relieving the symptoms of OA, and preliminary evidence suggests some of these compounds may exert a favourable influence on the course of the disease .

Medicines from reputed companies, comprises of purified and standardized active ingredients, and not just powder or extract of herbs.

For example, active ingredients are isolated and the compounds are characterized by spectral evidence. 

The pyrazoline derivatives of Boswellic acid were screened for anti-inflammatory activity. 

The effect of active alkaloids of Boswellia (Salai Guggul) on the pathways of arachidonic cascade were studied, in that they inhibited the formation of prostaglandins and leukotrienes.

 Active ingredients were tested in patients with chronic inflammation where leukotrienes keep inflammation active. 

Remission occurred in 82% of patients, with the active ingredient Boswellia serrata ( Salai Guggul). 

Antioxidant action of glycowithanolides from Ashwagandha produces anti-stress, anti- ageing, immunomodulatory and anti-inflammatory effects. 

Gingerol-6, active ingredient of ginger has potent anti-inflammatory and antioxidant properties which are helpful in reducing damage to joints. 

Nitric Oxide (NO) has been recently implicated in the process of inflammation; anti-NO drugs are being developed for this. Studies indicate that Curcumin, an active ingredient of Turmeric is a scavenger of NO and thus is an anti-inflammatory.

All these benefits  put together provide real disease modification which is reflected in reduction of biological markers.

Activated articular chondrocytes produce large amounts of nitric oxide (NO), and there is increasing evidence that this is involved in the etiopathogenesis (genesis) of osteoarthritis (OA).

Because of its short half- life, the biological effects of endogenously produced nitric oxide are likely to occur locally within the cartilage.

We have observed that inhibitors of nitric oxide synthases relieve the inhibition of matrix synthesis that otherwise occurs in response to IL-l.

To avoid the use of inhibitors, we have recently transduced chondrocytes with the iNOS (NOS-2) gene and confirmed the ability of the endogenously produced nitric oxide to inhibit matrix synthesis.

Despite the high levels of nitric oxide made by these cells, there was no

Nitric oxide was also shown to inhibit the production of TGF-beta by cells treated with IL- 1, as well as to decrease matrix production in response to IGF-1.

The hypothesis that nitric oxide inhibits matrix production by interfering with important autocrine and paracrine factors should be entertained.

Heparan sulfate proteoglycans produced by vascular endothelium may function physiologically to restrain the migration, multiplication, and phenotypic transition of vascular smooth-muscle cells, and to maintain an anticoagulant luminal surface by bonding and activating antithrombin III.

Thus, ample production of heparan sulfate proteoglycans may act to prevent atherosclerosis and its thrombotic complications.

The ability of exogenous heparin to stimulate synthesis of heparan sulfate proteoglycans by vascular endothelium may be largely responsible for the positive outcomes of most controlled evaluations of low-dose heparin as a long-term therapy for coronary disease.

Glucosamine, a biosynthetic precursor of mucopolysaccharides, can substantially enhance mucopolysaccharides production when added to cultured fibroblasts or chondrocytes;

The clinical utility of oral glucosamine in osteoarthritis may reflect increased synthesis of cartilage proteoglycans.

It is reasonable to speculate that exogenous glucosamine will likewise enhance heparan sulfate proteoglycans production by vascular endothelial cells, and, when administered orally in regimens comparable to those effective in osteoarthritis, will thereby act to retard atherogenesis .

Long-acting chondroprotective drugs have a symptomatic effect.

They are only effective in subjects with osteoarthritis and have no pure pain relieving effect.

They act within several weeks, improve Functional manifestations and have a remnant effect .

Chondroitin sulphates 4&6 are , glycosaminoglycans which participate in the matrix structure of cartilage.

They are well absorbed after oral intake.

They have a dose-dependent inhibitor effect in vitro on proteoglycan and collagen catabolism and have been shown to stimulate matrix synthesis.

Several clinical studies have demonstrated the chondroprotective efficacy of chondroitin sulphate 4&6 in osteoarthritis involving the hip, knee and finger joints.